Peripheral and Central Sensitization as Risk Factors of Low Back Pain
Hermann O. Handwerker
Acute low back pain is one of the most common complaints of adult humans, probably due to degenerative and/or use-dependent damages of the vertebral column and surrounding structures. When low back pain becomes chronic, it is a disabling disease. Chronic low back pain (CLBP), probably the most common chronic pain disease, is very difficult to treat (see Chapter 25). Though pathological processes at and around the vertebral column are the source of the pain, there is surprisingly little correlation between the magnitude e.g. of degenerative alterations of the spine and the pain intensity.
Chronic pain states are generally due to a complex interplay between peripheral and central nociceptive mechanisms. In CLBP this interplay is particularly complex, since it includes not only sensitized nociceptors from vertebrae, muscles, tendons, and small joints, but very often also has neuropathic components from damaged vertebral nerve roots. Sensitized nociceptors, or damaged axons, may bombard the central nervous system and this may lead to a disordered matrix of central nociceptive neuronal populations. In this respect, marked differences exist between muscle and skin nociceptors. Muscle pain has a much stronger tendency to be referred and to become chronic and this tendency is particularly strong in low back muscles (Taguchi et al. 1985, 1986). In addition, nocifensive reflexes may induce inadequate contractions of the spinal musculature which again create a changed micro-environment of the nociceptor terminals and hence lead to further nociceptor sensitization.
This short review of the pathophysiology of CLBP concentrates on three sources of chronic pain:
- 1) Nociceptor sensitization and damage.
- 2) Altered processing at central synapses.
- 3) Changes of the reactivity and structure of the brain in chronic pain states.
Indirect influences, e.g. the role of hormonal processes are covered by another chapter of this book (see Chapter 5) and only marginally implemented in this review. Details about the interaction of muscle activation and CLBP are discussed in two other chapters of this book (see Chapters 8 and 9).